I will be visiting my GP soon with blood test results that I had done privately. My Antibodies, which have never been tested by my GP are extremely high and I was told I should see my doctor as matter of urgency. They think I have Hashimotos disease. From my research, I don't think there's an awful lot you can do with Hashimotos and Im not sure what I would need to see the GP urgently about.
Can anyone explain how I should mention this to the GP and what he might want to do about it? I have never seen an endocrinologist. Should I insist on seeing one.
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Numberone1
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There isn't much your GP can do about antibodies, I'm afraid. I think the "matter of urgency" thing is probably for those whose GPs haven't already diagnosed as hypothyroid - I believe it's been known that you are for some time?
Some say that going gluten free has reduced their antibodies, some don't see as much success.
Yes it has been known I have hypothyroidism for some time. I guess Im more worried about what other auto immune diseases I might get with these antibodies especially as one of my daughters is t ype 1 and my aunt has coeliacs. I didn't know if there was something I could do to lower the antibodies. I believe LDN is a possibility?
Numberone1, if it's Hashimoto's antibodies that are high - TPOab and/or TgAB - then they only attack the thyroid gland. They won't give you diabètes or any other autoimmune disease.
That is not to say you won't develope other autoimmune antibodies, but the Hashi's one's are not a threat to anything else.
Although there is at least one interesting possibility - but read the underlined bit.
CNS Drugs. 2007;21(10):799-811.
Hashimoto's encephalopathy : epidemiology, pathogenesis and management.
Mocellin R1, Walterfang M, Velakoulis D.
Author information
1Neuropsychiatry Unit, The Royal Melbourne Hospital, Parkville, Victoria, Australia. Ramon.Mocellin@nh.org.au
Abstract
Hashimoto's encephalopathy is a term used to describe an encephalopathy of presumed autoimmune origin characterised by high titres of antithyroid peroxidase antibodies. In a similar fashion to autoimmune thyroid disease, Hashimoto's encephalopathy is more common in women than in men. It has been reported in paediatric, adult and elderly populations throughout the world. The clinical presentation may involve a relapsing and remitting course and include seizures, stroke-like episodes, cognitive decline, neuropsychiatric symptoms and myoclonus. Thyroid function is usually clinically and biochemically normal.Hashimoto's encephalopathy appears to be a rare disorder, but, as it is responsive to treatment with corticosteroids, it must be considered in cases of 'investigation negative encephalopathies'. Diagnosis is made in the first instance by excluding other toxic, metabolic and infectious causes of encephalopathy with neuroimaging and CSF examination. Neuroimaging findings are often not helpful in clarifying the diagnosis. Common differential diagnoses when these conditions are excluded are Creutzfeldt-Jakob disease, rapidly progressive dementias, and paraneoplastic and nonparaneoplastic limbic encephalitis. In the context of the typical clinical picture, high titres of antithyroid antibodies, in particular antithyroid peroxidase antibodies, are diagnostic. These antibodies, however, can be detected in elevated titres in the healthy general population. Treatment with corticosteroids is almost always successful, although relapse may occur if this treatment is ceased abruptly. Other forms of immunomodulation, such as intravenous immune-globulin and plasma exchange, may also be effective. Despite the link to autoimmune thyroid disease, the aetiology of Hashimoto's encephalopathy is unknown. It is likely that antithyroid antibodies are not pathogenic, but titres can be a marker of treatment response. Pathological findings can suggest an inflammatory process, but features of a severe vasculitis are often absent. The links between the clinical pictures, thyroid disease, auto-antibody pattern and brain pathology await further clarification through research. It may be that Hashimoto's encephalopathy will be subsumed into a group of nonvasculitic autoimmune inflammatory meningoencephalopathies. This group may include disorders such as limbic encephalitis associated with voltage-gated potassium channel antibodies. Some authors have suggested abandoning any link to Hashimoto and renaming the condition 'steroid responsive encephalopathy associated with autoimmune thyroiditis' to better reflect current, if limited, understanding of this condition.
OK, Don't think my brain is working very well tonight, but does the underlined bit mean that the antibodies themselves do not cause destruction of the thyroid gland, it's the inflammation that does it? And/or Don't cause Hashimoto's encephalopathy?
Is Hashimoto's encephalopathy called thus because Mr Hashimoto discovered it? Or because it involves the same antibodies as Hashimoto's thyroiditis?
It says that in the case of Hashimoto's encephalopathy, thyroid function is 'normal'. But, does that mean that the antibodies chose between the brain and the thyroid gland? Or does it mean that their definition of 'normal' isn't the same as ours?
Please be gentle with me in your answers, I've already been called thick and ignorant once today, and I think that's enough for one day! lol
Whatever else I might call you, the phrase "thick and ignorant" isn't going be be used.
It is called Hashimoto's Encephalopathy because of the same antibodies.
I have long questioned whether the
Thyroid Peroxidase antibodies actually do any attacking or destroying of the thyroid gland. One of the very earliest thyroid documents I ever read described them as indicators rather than causative. I have never been convinced otherwise.
One of the critical issues is that TPOab are found in the cerebro-spinal fluid. I can't remember the details - and the numbers, and whether they are found there in Hashimoto's Thyroiditis.
I think the "normal" thyroid is meant to be taken as saying that you could have the encephalopathy without having obvious hypothyroid symptoms or blood test results. Whether that is a complete all clear or not is another matter.
OK, so what about the Tg antibodies? Do they damage the gland? If not, why does the gland shrink? And what's this story about little bits of the gland breaking off and releasing its hormone into the blood making you go 'hyper'? Which is what we've all been told - and tell others, come to that.
My interpretation (and I would be very happy to be corrected by reference to good research) is that thyroglobulin usually exists only within the thyroid gland.
When that gland is damaged, some thyroglobulin spills into the blood stream. Thyroglobulin antibodies are then released by the immune system to get rid of the "foreign" substance.
As I understand, thyroglobulin is a protein which would not normally be accessible to any antibodies in the bloodstream. Only spillage would cause it to be released.
That spillage could be from physical damage (including thyroid surgery), or because the cells of the thyroid are attacked by macrophages. Maybe even normal cells turnover occasionally releases a small amount?
My understanding is that lymphocytes infiltrate the thyroid gland and cause the damage and inflammation. Lymphocytes are a subset of white blood cells which are supposed to fight off virus and bacterial infection but something goes awry and instead of fighting infection they turn on the thyroid gland. Thyroid peroxidase and thyroglobulin antibodies are a response to the lymphocyte infiltration not the cause.
Damaged thyroid cells dump hormone as they die off which causes transient hyperthyroidism and repeated lymphocyte attacks and cell die off atrophies the thyroid gland.
There's nothing your GP or an endo will be able to do about Hashimoto's. They treat the hypothyroidism caused by Hashimoto's with Levothyroxine. Many Hashi patients find adopting 100% gluten-free diet helps reduce Hashi symptoms and antibodies but it doesn't work for everyone.
I am not a medical professional and this information is not intended to be a substitute for medical guidance from your own doctor. Please check with your personal physician before applying any of these suggestions.
I think my hyper/ hypo symptoms are from hasmistos ... Feel like am on a roller coaster ... My Levo ( 100mg ) helps ... But can feel my body going up and down !!!! ...think started from virus in January leaving me tickly cough and other probs .... Thought radio iodine was end of my probs 3 years ago ..... Wrong !!!
If you had RAI because you had Graves it is possible for the thyroid to regenerate and produce hormone so you should ask for a thyroid function test including FT3 to check that you aren't producing hormone in addition to the 100mcg. Your GP can test thyroid peroxidase antibodies as the same time to determine whether you have autoimmune thyroid disease (Hashimoto's) as well as Graves although s/he may decline to do so as you are now being treated for hypothyroidism.
I am not a medical professional and this information is not intended to be a substitute for medical guidance from your own doctor. Please check with your personal physician before applying any of these suggestions.
They just keep saying my t3 , t4 and tsh are in normal range. ( whatever that is !!! ) .... Have heard early stages of hashimotos doesn't show straight away .... Could explain why I had bad reaction to Levo other day if my body doesn't need it. !!! They never said if still producing hormones !!! ... Will get the antibodies done too ... God I am so glad I found you all !!!
Normal simply means results are in range. There is often room to tweak dose to optimise results. It's guesswork whether or not you need 100mcg, less or more without seeing your thyroid results and ranges. If you want advice on your results please post them in a new post by clicking on Write a post and members will comment.
I went totally gluten free back in September last year and my antibodies are reducing nicely. They are not within the lab range yet but I'm very hopeful. Going GF isn't difficult either once you get going. It was inflammatory arthritis that made me decide to do it - I've got Graves Disease and a few other autoimmune conditions so it seemed like a good idea at the time, I mentioned it to a doctor I saw at my surgery and didn't get any reaction so I've stuck with it.
I have to say that my arthritis is always worst if I eat gluten. I had been gluten free (almost 100%) for about a year, then came Christmas, then holidays in the US, then Easter and I am suffering.
Gluten definitely causes inflammation in me. Is that what happens to you?
I don't know that I feel all that different it's hard to tell because I'm taking hydroxychloroquine for my arthritis but I can see the reduction when I do a Blue Horizons thyroid test that shows my antibodies.
I haven't knowingly had anything with gluten in it - I don't want to take any chances while things are looking good. I certainly missed good old stodgy hot cross buns last week, I had a GF one but it just wasn't the same at all, not worth eating really. It spiked my blood sugar up compared to normal food and it wasn't even all that good.
What do you think of the drug you take for arthritis. Im going to my GP soon with my list of questions and hadn't heard of the drug you're on. Im sick of being in pain and don't like to take many pain killers. Does this one help?
I started with three months on steroids which took away ALL the pain I was in - muscular and joints - then after a month I went onto 200mg hydroxychloroquine (Quinoric) - they say it can take several weeks to kick in and I would agree with that.
When I stopped the steroids in December I could still 'feel' a few achy places but after a few weeks it settled down quite nicely.
I still get odd days when I feel a bit of an ache but nothing like before and I can also do all the things that I couldn't do before - for example I can now pull out plugs, press my inhaler in the normal way, all sorts of things.
I don't think hydroxy works for everyone though but from what I've read there are lots of other drugs they could try - in my case I think from looking at the patient information leaflet I could even take 400mgs a day. I'm due to go back to the rheumy at the end of April so I'll probably know more then.
Some people think that going Gluten Free hasn't worked if after a few months there has not been any improvement in the reduction of anti-bodies. Again we are all different - and mine have only just reduced after 11 years since diagnosis/treatment. The decrease only happened during the third year of being gluten free !
Going gluten free is beneficial for many conditions and not just the thyroid. It seems gluten can cause an inflammatory response in the gut. Am afraid when it come to the thyroid there is no quick fix......
To the right of this page there is a heading - Topics. Under the heading scroll down for Hashimotos - 1700+ posts - so lots of reading and information ......
Am not a Doc - just a Hashi's girl - with Crohns and a B12 issue.
Some 6 years ago I had been told by the hospital that I had a 'red flag' warning of a Thyroid problem and it was suggested that I should see my GP. He did a blood test and since my TSH was 7 he would not treat me until it was 10 or above. I went surfing and was advised that I should check for antibodies and if they were present I should be treated with a TSH over 5. Like you I had a private blood test done and this proved antibodies of just over 1000. Went back to GP and shoved the report under his nose and he blustered and finally agreed to give me a trial of Levothyroxine of 25 mg , this was increased after a couple of months to 75 mg and has remained stable ever since. As others have said its the Hypo/hyperthyroid that's treated and not the antibodies, there isn't much your can do about the antibodies. I did try gluten free for a while but since it played havoc with my blood sugars I gave up.
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